The physical factors affecting the production of an organic solvent-tolerant protease from Pseudomonas aeruginosa strain K was investigated. Growth and protease production were detected from 37 to 45 degrees C with 37 degrees C being the optimum temperature for P. aeruginosa. Maximum enzyme activity was achieved at static conditions with 4.0% (v/v) inoculum. Shifting the culture from stationary to shaking condition decreased the protease production (6.0-10.0% v/v). Extracellular organic solvent-tolerant protease was detected over a broad pH range from 6.0 to 9.0. However, the highest yield of protease was observed at pH 7.0. Neutral media increased the protease production compared to acidic or alkaline media.

Pulmonary surfactant has two distinct functions within the lung: reduction of surface tension at the air-liquid interface and participation in innate host defense. Both functions are dependent on surfactant-associated proteins. Pseudomonas aeruginosa is primarily responsible for respiratory dysfunction and death in cystic fibrosis patients and is also a leading pathogen in nosocomial pneumonia. P. aeruginosa secretes a number of proteases that contribute to its virulence. We hypothesized that P. aeruginosa protease IV degrades surfactant proteins and results in a reduction in pulmonary surfactant host defense and biophysical functions. Protease IV was isolated from cultured supernatant of P. aeruginosa by gel chromatography. Incubation of cell-free bronchoalveolar lavage fluid with protease IV resulted in degradation of surfactant proteins (SP)-A, -D, and -B. SPs were degraded in a time- and dose-dependent fashion by protease IV, and degradation was inhibited by the trypsin-like serine protease inhibitor Nalpha-p-tosyl-L-lysine-chloromethyl ketone (TLCK). Degradation by protease IV inhibited SP-A- and SP-D-mediated bacterial aggregation and uptake by macrophages. Surfactant treated with protease IV was unable to reduce surface tension as effectively as untreated surfactant, and this effect was inhibited by TLCK. We speculate that protease IV may be an important contributing factor to the development and propagation of acute lung injury associated with P. aeruginosa via loss of surfactant function within the lung.

You go get em! Thank you for what you are doing.
You have the goods on em. And for all you have gone through, I am amazed. But, when depression turns back to anger and then we can actually approach these people, even though they may answer in froggy ways, and jump over the truth, that good ole L'anna Voo might come in handy.

Oh my, we must get back to it as our Nadas says.

Okay, now that pseudomonas aerug.....can we get a good picture of that? For comparison?

The V antigen, or LcrV (for low calcium response V), is a secreted protein that is thought to help in multiple functions of the Type III secretion system of plague, including regulation of the Yop virulence factors. Importantly, it is thought to be essential for plague pathogenesis and the onset of the low calcium response.
It is also thought to function as an immunomodulator by inhibiting
production of pro-inflammatory cytokines such as interferon-gamma
" S C A L A R "
and tumor necrosis factor-alpha. One theory points to a role for V antigen in eliciting anti-inflammatory IL-10 production by host immune cells, thereby inhibiting production of pro-inflammatory cytokines and preventing a systemic immune response.
Among other data, mice infected with avirulent plague that lacked
the plasmid that bears the V antigen showed a robust TNF-alpha and IFN-gamma response. Co-administration of pure V-antigen exacerbated infections of Listeria monocytogenes and Salmonella typhimurium in mice.
Co-administration of IFN-gamma and TNF-alpha helped protect against 10
minimal lethal doses of lcrV+ plague bacteria. As a recent review stated, “the generalized Yersinia-induced paralysis of professional phagocytes that occurs in vivo is caused by the systemic down- regulation of inflammation,” putatively by IL-10.
The same review argues that the role of the V-antigen as a “long-range missile capable of systemic immunosuppression” is what separates Yersinia pestis from its enteropathogenic and chronic disease inducing cousins Y. enterocolitica and Y. pseudomonas as well as from the more innocuous Pseudomonas aeruginosa, which bears a homologous protein (PcrV). Of course, the role for the V-antigen as one of the (if not the) chief immunosuppressants in plague is under considerable debate.

"Pseudomonas aeruginosa is a Gram-negative bacterium that is noted for its environmental versatility, ability to cause disease in particular susceptible individuals, and its resistance to antibiotics. The most serious complication of cystic fibrosis is respiratory tract infection by the ubiquitous bacterium Pseudomonas aeruginosa. Cancer and burn patients also commonly suffer serious infections by this organism, as do certain other individuals with immune systems deficiencies. Unlike many environmental bacteria, P. aeruginosa has a remarkable capacity to cause disease in susceptible hosts. It has the ability to adapt to and thrive in many ecological niches, from water and soil to plant and animal tissues. The bacterium is capable of utilizing a wide range of organic compounds as food sources, thus giving it an exceptional ability to colonize ecological niches where nutrients are limited. P. aeruginosa can produce a number of toxic proteins which not only cause extensive tissue damage, but also interfere with the human immune system's defense mechanisms. These proteins range from potent toxins that enter and kill host cells at or near the site of colonization to degradative enzymes that permanently disrupt the cell membranes and connective tissues in various organs. This bacterium is also noted for its resistance to many antibiotics.

P. aeruginosa is widely studied by scientists who are interested in not only its ability to cause disease and resist antibiotics, but also its metabolic capability and environmental versatility. Analysis of its genome sequence has identified genes involved in locomotion, attachment, transport and utilization of nutrients, antibiotic efflux, and systems involved in sensing and responding to environmental changes.

A major interest of pharmaceutical companies, such as Chiron*, is to learn more about the genes of P. aeruginosa and other disease-causing bacteria in order to better understand the physiology of these organisms. These insights will be used to develop new antibacterial drugs to successfully treat infections by bacteria like P. aeruginosa that are resistant to many of today’s antibiotics. ...
...
*PathoGenesis Corporation, who played a major role in sequencing the first P. aeruginosa genome, is now a part of Chiron and continues its interest in the development of new anti-Pseudomonad drugs."

"The pseudomonads are better known to microbiologists as pathogens of plants rather than animals, but three Pseudomonas species are pathogens of humans. Pseudomonas aeruginosa is an opportunistic pathogen that causes urinarytract infections, respiratory system infections, dermatitis, soft tissue infections, bacteremia and a variety of systemic infections, particularly in victims of severe burns, and in cancer and AIDS patients who are immunosuppressed. Pseudomonas aeruginosa is occasionally a pathogen of plants, as well. Pseudomonas mallei causes a disease in horses known as glanders. It is a true parasite, since it is unable to survive in nature in the absence of its host. The primary focus of infection is the lungs. The disease can be transmitted to humans from the horse. Pseudomonas pseudomallei is the agent of melioidosis, a highly fatal tropical disease of humans and other mammals. It is also an opportunistic pathogen contracted through the contamination of wounds with mud or soil.

The typical Pseudomonas bacterium in nature might be found in a biofilm, attached to some surface or substrate, or in a planktonic form, as a single cell actively motile my means of polar flagella. Pseudomonas is one of the most vigorous, fast-swimming bacteria seen in hay infusions and pond water samples. Pseudomonas aeruginosa is motile by means of a single polar flagellum. P. aeruginosa can live in a sessile biofilm form, or it can live in a planktonic form, as a free-swimming cell.

Pseudomonas aeruginosa is not particularly distinctive as a pseudomonad, but there are a few characteristics that are noteworthy and relate to its pathogenesis. The organism can be isolated from soil and water, particularly in enrichments for denitrifying bacteria. Although the bacterium is respiratory and never fermentative, it will grow in the absence of O2 if NO3 is available as a respiratory electron acceptor. P. aeruginosa possesses the metabolic versatility for which pseudomonads are so renowned. Organic growth factors are not required, and it can use more than thirty organic compounds for growth. Pseudomonas aeruginosa is often observed growing in "distilled water" which is evidence of its minimal nutritional requirements. Its optimum temperature for growth is 37 degrees, and it is able to grow at temperatures as high as 42 degrees. Its tolerance to a wide variety of physical conditions, including temperature, contributes to its ecological success as an opportunistic pathogen. Pseudomonas aeruginosa does, however, show a predilection for growth in moist environments, a reflection of its natural existence in soil and water.

P. aeruginosa isolates may produce three colony types. Natural isolates from soil or water typically produce a small, rough colony. Clinical samples, in general, yield one or another of two smooth colony types. One type has a fried-egg appearance which is large, smooth, with flat edges and an elevated appearance. Another type, frequently obtained from respiratory and urinarytract secretions, has a mucoid appearance, which is attributed to the production of alginate slime.The smooth and mucoid colonies are presumed to play a role in colonization and virulence.......

So, this alginate slime is not a good thing....now is it, but .....give it to the kids.

What got me about this article is that ole Glanders keeps coming back......

It was used as a bioweapon in WWI. Expansion upon that probably didn't take much........

"Pyocyanin (from "pyocyaneus") refers to "blue pus" which is a characteristic of suppurative infections caused by Pseudomonas
aeruginosa."

LONDON: look at this and they tell us we have Rheumatoid Arthritis. Right! NOT! This stuff is horrible, and yet, it is not serious to the CDC?
Is that because the cocktail is even worse than just this?

"These bacteria are clinically important because they are resistant to most antibiotics and they are capable of surviving in conditions that few other organisms can tolerate.".....

MORE PROOF:
"The lipopolysaccharide layer helps the cell adhere to host tissues and prevents leukocytes from ingesting and lysing the organism. Lipases and exotoxins then procede to destroy host cell tissue which then leads to the complications associated with infection. " LPS anyone?

OOOOOOOHHHHHHMY.......bringing up some old handles here......

"OTHER SPECIES
Burkholderia (Pseudomonas) cepacia is an opportunistic pathogen of cystic fibrosis patients. It also shows substantially greater antibiotic resistance than its relative, P. aeruginosa. However, B. cepacia can be distinguished from Pseudomonas species because it is lysine positive.

Although not of the same genus, Stenotrophomonas maltophila (formerly known as Xanthomonas maltophila) is very similar to the Pseudomonads. This motile bacterium is a cause of nosocomal infections in immunocompromised patients. S. maltophila also harbors significant resistance to many antibiotics considered effective for treating Pseudomonas infections. However, most strains of the bacterium are susceptible to trimethoprim sulfamethoxazole. S. maltophila can also be distinguished from Pseudomonas species by the lysine and DNAse tests for which it is positive "

Found a bioshield thing, but , naaaaaaaahhhh....that couldn't be in the plague from the chemtrails?
Wonder how those pilots keep that all straight up there, in their bio suits.
I think that is why they also clean off the regular jets we fly on.
Ice on the wings.........oh yeah, looks like ice, feels like ice, but clings like spider webs.
Saw the strangests clouds, dark clouds bumping into each other, wonder how the weather gets so violent lately? Scaler could help that......
Okay then.........well........

"Association of the PilZ domain with a variety of other domains, including likely components of bacterial multidrug secretion system, could provide clues to multiple functions of the c-di-GMP in bacterial pathogenesis and cell development"

"We have identified and characterized two P. aeruginosa pathogenicity islands (PAPI-1 and PAPI-2) in the genome of PA14, a highly virulent clinical isolate. The 108-kb PAPI-1 and 11-kb PAPI-2, which are absent from the less virulent reference strain PAO1, exhibit highly modular structures, revealing their complex derivations from a wide array of bacterial species and mobile elements. Most of the genes within these islands that are homologous to known genes occur in other human and plant bacterial pathogens. For example, PAPI-1 carries a complete gene cluster predicted to encode a type IV group B pilus, a well known adhesin absent from strain PAO1. "

Proteins containing GGDEF domains are encoded in the majority of sequenced bacterial genomes. In several species, these proteins have been implicated in biosynthesis of exopolysaccharides, formation of biofilms, establishment of a sessile lifestyle, surface motility, and regulation of gene expression. However, biochemical activities of only a few GGDEF domain proteins have been tested. These proteins were shown to be involved in either synthesis or hydrolysis of cyclic-bis(3'-->5') dimeric GMP (c-di-GMP) or in hydrolysis of cyclic AMP. To investigate specificity of the GGDEF domains in Bacteria, six GGDEF domain-encoding genes from randomly chosen representatives of diverse branches of the bacterial phylogenetic tree, i.e., Thermotoga, Deinococcus-Thermus, Cyanobacteria, spirochetes, and alpha and gamma divisions of the Proteobacteria, were cloned and overexpressed. All recombinant proteins were purified and found to possess diguanylate cyclase (DGC) activity involved in c-di-GMP synthesis. The individual GGDEF domains from two proteins were overexpressed, purified, and shown to possess a low level of DGC activity. The oligomeric states of full-length proteins and individual GGDEF domains were similar. This suggests that GGDEF domains are sufficient to encode DGC activity; however, enzymatic activity is highly regulated by the adjacent sensory protein domains. It is shown that DGC activity of the GGDEF domain protein Rrp1 from Borrelia burgdorferi is strictly dependent on phosphorylation status of its input receiver domain. This study establishes that majority of GGDEF domain proteins are c-di-GMP specific, that c-di-GMP synthesis is a wide-spread phenomenon in Bacteria, and that it is highly regulated.

RECEIVER AND REGULATOR. AND what about
DIFFRACTOR? in following. This was pub in 1981.

"The polar pili of Pseudomonas aeruginosa strains K and O are hollow cylinders with 52 Å outer diameter and 12 Å inner diameter. There is a girdle of low electron density (interpreted as due to a local concentration of hydrophobic amino acid side-chains) centred at 31 Å diameter. Similar X-ray diffraction patterns are obtained from oriented fibres of the two types of pili, to a resolution of 7 Å in the equatorial direction and 4 Å in the meridional direction. The two types of pilin protein subunits have a similar molecular weight, and their sequences contain a number of homologous regions. They form a helical array with 4.06 to 4.08 units per turn of a basic helix that has a pitch of 40.8 Å for strain K pili and 41.3 Å for strain O pili at 75% relative humidity. A method is described for distinguishing between very similar diffraction patterns.

There is strong intensity at 10 Å near the equator and at 5 Å near the meridian on the diffraction patterns. This intensity distribution is characteristic of α-helical rods running roughly in the direction of the fibre axis. The orientation of these rods was established by the fit between the transform of an α-helical polyalanine model and the strong near-equatorial layer-line. '
SOURCE:
http://www.sciencedirect.com/science?_o ... d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=9522a6a88910d7a0944902301777d6e9

Are we talking diffraction in magnetic core of earth?
per species orientation? The caps here, are they in Anstroms? (sp).